The Role of Toll-Like Receptors (TLR) in Infection and Inflammation

Toll-like receptors (TLRs) represent a powerful system for the recognition and elimination of pathogen-associated molecular patterns (PAMPs) from bacteria, viruses, and other pathogens and damage-associated molecular patterns (DAMPs) released from dying cells. Typical PAMPs include bacterial cell wa...

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Bibliographic Details
Format: eBook
Language:English
Published: Basel MDPI - Multidisciplinary Digital Publishing Institute 2023
Subjects:
AKT
hop
LPS
n/a
TLR
Online Access:Open Access: DOAB: description of the publication
Open Access: DOAB, download the publication
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520 |a Toll-like receptors (TLRs) represent a powerful system for the recognition and elimination of pathogen-associated molecular patterns (PAMPs) from bacteria, viruses, and other pathogens and damage-associated molecular patterns (DAMPs) released from dying cells. Typical PAMPs include bacterial cell wall components, viral pathogens, or pathogenic nucleic acids, including viral RNA and DNA. Activation of TLRs leads to the production of proinflammatory cytokines and type I interferons which are important for the induction of the host immune response against bacterial and viral infections. However, dysregulation and overstimulation can be detrimental, leading to hyper-inflammation, sepsis, and loss of tissue integrity. The involvement of TLRs in inflammation and bacterial infection has been recognized for a long time. There is an increasing number of reports demonstrating the involvement of TLR activation in a variety of viral infections, associated with protective immunity, but also immune hyper activation and even viral replication. Recent data show the involvement of TLR activation in various acute respiratory viral infections, including SARS-CoV-2 and indicate an essential role in COVID-19 pathology. It aimed to gather newest data and hypotheses regarding molecular and cellular mechanisms of TLR triggering and activation and their downstream signaling pathways by viral infections, and their correlation to immunology and pathophysiology of the associated diseases, to facilitate translational research resulting in new targets for the treatment of viral infectious diseases including COVID-19. 
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653 |a 2'-O-ribose-methylation 
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653 |a AKT 
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653 |a alveolar macrophages 
653 |a antiviral 
653 |a antiviral agent 
653 |a aquaporin-3 (AQP3) 
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653 |a CD14 
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653 |a COVID-19 
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653 |a diabetes 
653 |a endocytosis 
653 |a glucose 
653 |a hepatitis C virus 
653 |a histone deacetylase inhibitor 
653 |a hop 
653 |a human PDL 
653 |a immune activation 
653 |a immune system 
653 |a immunoregulation 
653 |a immunotherapy 
653 |a infection 
653 |a inflammation 
653 |a inflammatory 
653 |a innate immunity 
653 |a keratinocytes 
653 |a lipopolysaccharide (LPS) 
653 |a LPS 
653 |a MAPKs 
653 |a monoclonal antibody TLR4 
653 |a MUC1 (Mucin 1) 
653 |a n/a 
653 |a NF-kappaB 
653 |a nucleolin 
653 |a oligonucleotide 
653 |a Omicron 
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653 |a RNA therapeutics 
653 |a RNase T2 
653 |a SARS-CoV-2 
653 |a sepsis 
653 |a septic shock 
653 |a skin 
653 |a sncRNA 
653 |a spike protein 
653 |a sterile inflammation 
653 |a TLR 
653 |a TLR4 
653 |a TLR4-RAGE crosstalk 
653 |a TLR7 
653 |a TLR7 (Toll-like receptor 7) 
653 |a TLR8 
653 |a Toll-like receptor 
653 |a Toll-like receptor (TLR) 
653 |a toll-like receptor-2 (TLR2) 
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653 |a virus entry 
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